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Updated: Oct 9, 2026

Histological Examination of Mitochondrial Morphology in a Parkinson's Disease Model
Published on: June 23, 2023
Further evidence for mitochondrial dysfunction in progressive supranuclear palsy
D S Albers1, R H Swerdlow, G Manfredi
1Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, New York 10021, USA. daa2010@mail.med.cornell.edu
Abstract:
Recent data from our laboratory have identified a role for mitochondrial dysfunction in the pathogenesis of progressive supranuclear palsy (PSP). To extend this finding, we measured key parameters of mitochondrial function in platelet-derived cytoplasmic hybrid (cybrid) cell lines expressing mitochondrial genes from patients with PSP. We observed significant decreases in aconitase activity, cellular ATP levels, and oxygen consumption in PSP cybrids as compared to control cybrids, further suggesting a contributory role of impaired mitochondrial energy metabolism in PSP, possibly due to genetic abnormalities of mitochondrial DNA.
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